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Microbiology > Antimicrobials and Antimicrobial Resistance > Flashcards

Antimicrobials and Antimicrobial Resistance Flashcards

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Biology 101 flashcards
1
Q

what is virulence

A

how pathogenic an organism is

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2
Q

what are antibiotics

A

limit the growth of microorganisms

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3
Q

first modern antibiotics were

A

synthetic

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4
Q

treatment of syphilis

A

ehrlich screen arsenic-containing compounds

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5
Q

bacteria that creates syphilis

A

Treponema pallidum

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6
Q

synthetic antibiotics in use today

A

sulfa drugs, quinolines, oxazolidinones

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7
Q

who came up with the first modern antibiotics

A

paul ehrlich

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8
Q

who discovered the first natural antibiotic and how

A

alexander fleming
observed an area of no bacterial growth on a plate surrounding some mould

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9
Q

when was the first patient treatment

A

1942

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10
Q

howard florey and ernst chain developed

A

penicillin production on industrial scales

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11
Q

hodgkin discovered

A

structure of penicillin

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12
Q

what did the discovery of structure of penicillin allow for

A

-rational chemical modification
-semi-synthetic antibiotics
-promote stability, reduce toxicity, enhance potency

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13
Q

what is a major source of antibiotics

A

streptomyces

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14
Q

streptomyces

A

soil bacteria: gram-positive, filamentous bacillus, aerobic and spore-forming
elaborate secondary metabolism
looks more like a fungi than a bacteria
produce geosmin: smell of rain
produce 2/3 of clinical useful antibiotics ending in -mycin

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15
Q

antibiotics are often

A

secondary metabolites

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16
Q

what is not required for homeostasis

A

secondary metabolism

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17
Q

secondary metabolites are produced during

A

stationary phase

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18
Q

secondary metabolites can have

A

unusual, complex chemical structures

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19
Q

bactericidal

A

kill bacteria

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20
Q

bacteriostatic

A

prevent the growth of bacteria

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21
Q

no new class of antibiotics have been developed in

A

15-20 years

22
Q

antibiotic development is

A

slow and expensive

23
Q

crowded plate technique

A

plate dilute solution of soil bacteria on a plate and look for zones of inhibition

24
Q

effective antibiotics should selectively target

A

bacterial structures/metabolism but not mammalian

25
Q

antibiotic effectiveness depends on

A

physiology of target bacteria

26
Q

targets of antibiotics - gram positive cell wall synthesis

A

requires crosslinking of peptidoglycan for cell wall integrity

penicillin blocks insertion of interpeptide pentapeptide

penicillin resembles peptidoglycan subunit and binds penicillin-binding protein (transpeptidase)

this blocks the crosslinking enzyme and the cell wall cannot rebuild and it dies

27
Q

targets of antibiotics - bacterial cell membrane

A

polymyxin

binds to LPS
disrupts outer and inner membrane of gram-negative bacteria
leads to cell lysis

28
Q

targets of antibiotics - bacterial ribosomes

A

major classes of protein synthesis-inhibiting antibacterials:
chloramphenical, macrolides, lincosamides bind to large subunit and stops protein synthesis

aminoglycosides bind to small subunit and impairs proofreading, produces faulty proteins

tetracyclines bind to small subunit and blocks the binding of tRNAs to inhibit protein synthesis

29
Q

targets of antibiotics - nucleic acid synthesis

A

requires topoisomerases and gyrase to prevent supercoiling
quinolones inhibit the activity of DNA gyrase domains, causing supercoiling

30
Q

targets of antibiotics - metabolic pathways

A

blocks folic acid synthesis which is required for nucleotide synthesis

sulfonamide and trimethoprim are both antimetabolites

competitive inhibitors

31
Q

folic acid is _______ in bacteria, but is obtained through ____ in humans

A

synthesized
diet

32
Q

minimum inhibitory concentration

A

lowest does that inhibits bacteria growth

33
Q

minimum bactericidal concentration

A

lowest dose that kills bacteria

34
Q

MIC and MBC is important to

A

maintain an effective concentration of antibiotics in the body

35
Q

antibiotic resistance

A

efflux pump
blocked penetration
inactivation by enzymes
target modification

36
Q

antibiotic resistance - efflux pumps

A

solute pumps, requires ATP
removes amphipathic molecules from cytoplasm (bile salts)
broad substrate specificity

37
Q

antibiotic resistance - beta-lactamases

A

an enzyme that cleaves beta-lactam rings
ring present in penicillin-derived drugs
cleavage prevents proper targeting of drug

38
Q

acquiring antibiotic resistance genes

A

acquired vertically and horizontally
can be acquired by transformation, transduction or conjugation
core genomes of bacteria acquire mutations over time which can limit susceptibility to antibiotics
mutations quickly become fixed if there is no fitness cost or a benefit

39
Q

what is the fastest and most common means of spreading resistance

A

conjugation of plasmids
inter- and intraspecies

40
Q

ESKAPE pathogens

A

important targets for antibiotic development
common causes of nosocomial infections
found to be multidrug-resistant

41
Q

multidrug-resistant bacteria

A

are resistant to more than three classes of antibiotics

42
Q

biofilms limit

A

penetration of antibiotics and promote the spread of antibiotic resistance genes

43
Q

phage therapy

A

lytic phage kill bacteria during egress

difficult to match a phage with a particular strain of bacteria (must be permissive)

44
Q

antivirals

A

drugs target viral proteins during all phases of the replication cycle

45
Q

how do viruses change the cells

A

reprogram host cell metabolism
use cellular proteins for non-typical purposes

46
Q

antivirals - nucleic acid synthesis

A

works as chain-terminators
prevent new DNA chains from being formed

47
Q

chain-terminators

A

halt extension from 5’ to 3’ on new strand by lack of 3’ hydroxyl group

48
Q

antivirals- targeting proteases

A

act on both viral and host proteins

inhibitors resemble normal protease target, but lack cleavage site
prevents viruses from making copies of itself

49
Q

resistance to antivirals

A

high mutation rate
generate a large amount of progeny virions
co-infection of cells with multiple viruses is common
viral genomes can complement defects in co-infecting genomes
inhibited viruses are quickly selected against, leaving more host cells for resistant viruses

50
Q

resistance to antivirals: serine to aspargine

A

M2 ion channel is present in the influenza A virus envelope
allows protons to enter the virion to releease genome segments from M1 matrix protein
amantadine blocks the M2 ion channel inhibiting viral uncoating
a single AA change in the channel is sufficient to prevent Amantadine binding without loss of conductivity
mutation and resistance is now widespread

51
Q

combination therapy - HIV

A

HIV has an extremely high mutation rate
diversity from both viral polymerase and cystine deamination by host innate immune factor APOBEC3
anti-retrovirals target viral proteins
used in combinations or three or four to limit emergence of resistance
same strategy used to cure Hepatitis C virus

52
Q

targeting host proteins to limit SARS-CoV-2 replication

A

treat with increasing concentration of TMPRSS2 inhibitor, Camostat reduces infection
camostat prevented viral entry
camostat already approved for clinical use
difficult for viruses to evolve away from dependence on host targets

Microbiology (11 decks)

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